The central focus of this research protocol has been on the importance of resistance to insulin-mediated glucose disposal and compensatory hyperinsulinemia in modulation of metabolic changes that increase risk of coronary heart disease. Our specific aims are: 1) To establish the link between insulin resistance (and the cluster of abnormalities associated with this defect in insulin action), endothelium- dependent vasodilatation (endothelium-dependent vascular reactivity, EDVR), and determinants of endothelial-monocyte interaction. 2) To magnify the metabolic changes associated with Syndrome X by dietary manipulation in order to exxagerate their deleterious effects on endothelial dysfunction and monocyte-endothelial interaction.